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In the EEG after sleep deprivation paroxysms with spikes and spike wave-complexes as well as paroxysms with slow waves can be seen. The paroxysms occur either spontaneously (it means at any time during the record) or at moments of shifting vigilance. These moments are characterized by sudden changes of the EEG frequency for instance by transition from one sleep stage to another. Paroxysms with spikes or spike wave-complexes occur mainly at the transition from lower to higher levels of vigilance and are accompanied by abnormal K-complexes and abnormal photosensibility. Paroxysms of slow waves occur mainly at the transition from higher to lower levels of vigilance, abnormal K-complexes and abnormal photosensitivity are lacking but in some cases the before diffuse abnormal EEG is improved after sleep deprivation. It assumed that we are dealing with two different types of reaction.

19 patients were treated with valproic acid (VPR) in combination with classical anticonvulsants (phenytoin, phenobarbitone, primidone, carbamazepine). Patients with a mean serum concentration of 340 micron moles/l showed a marked improvement as to the frequency of seizures or were even completely free from seizures, provided that the other anticonvulsants were also given in the therapeutic range. Cases showing only a slight reduction in seizure frequency or no improvement had a mean serum level of 229 micron moles/l. This investigation shows that in severe cases of epilepsy treated by combined therapy all given anticonvulsants must reach therapeutic levels to achieve effective control of seizures in most patients.

In 35 patients intraoperative EEG-monitoring during carotid desobliteration under general anesthesia was performed. 15 of these patients had preoperatively focal EEG-changes, coinciding frequently with a cerebral infarct or with carotid changes also contralateral to the side of the desobliteration. 18 patients had during the carotid clamping EEG-changes (slowing of frequency and decrease in amplitude) or a worsening of preoperative changes. 15 of these patients had a complete recovery of these changes after unclamping. The EEG changes do occur more frequent in patients who had a cerebral infarct or bilateral carotid changes preoperatively. Since the EEG-changes during the carotid clamping do signal a critical lowering of the brain perfusion, an ischemic etiology has to be assumed. The use of a shunt during the procedure to prevent irreversible ischemic damage seems therefore to be justified.

The significance of serum lipid levels in the assessment of risk in ischaemic cerebral diseases is controversial. The differential investigation of lipoproteins, however, showed that the high-density lipoprotein (HDL) fractions are absolutely or relatively decreased with respect to low-density lipoproteins (LDL) in cerebral infarcts and in transient ischaemic attacks. Raised LDL/HDL ratios were found in this study, as an expression of a relative lowering in HDL, in ischaemic cerebral disease associated with pathological disorders of the large or small cerebral vessels. Hence, it appears that HDL represents a protection factor, not only in the prevention of cardiovascular, but also cerebrovascular disease and a decrease in HDL may be a risk factor.

Visual evoked potentials (VEP) were investigated in 12 members of a family with Charcot-Marie-Tooth disease, 7 of whom showed manifest clinical signs of the disease. The mean value of the latency P100 of VEP in the 12 patients did not differ significantly from the value in normal controls, nor did the values in members with considerably reduced nerve conduction velocities differ significantly from those in members with normal nerve conduction velocity. Among the investigated members of the family, however, there was a significant difference in mean P100 latency between family H.G. with no clinical signs of the disease and the family of the twin brother, F.G. with clear clinical and neurographic signs of HMSN I. The divergent opinions given in the literature may be explained by heterogeneity, as well as an extreme expression of the inherited defect and a combination of two independently inherited diseases.

Alcoholism and epileptic seizures frequently coincide. Two groups can be distinguished clinically and by EEG. In one group (group I), seizures occur only during a period of alcohol withdrawal or partial withdrawal and can only be explained because of alcoholism in the history of the patient. In the other group (group II), seizures occur spontaneously, as well as during alcohol withdrawal, and epileptogenic factors (residual brain damage, former epileptic seizures, and a family history of seizures) probably play an important role in the manifestation of the seizures. Paroxysms or focal abnormalities are rarely seen in group I; in group II, EEG abnormalities are seen approximately as frequently as in other epileptic conditions. Both groups were examined to determine the extent of their EEG abnormalities after 24 h of sleep deprivation. Before and after sleep deprivation, only 4% of 52 chronic alcoholic patients without epileptogenic risk factors had EEG foci. Of the 52, 2% before sleep deprivation and 8% after sleep deprivation had generalized paroxysms. Of 128 chronic alcoholic patients with additional epileptogenic factors, 19% before sleep deprivation and 24% after sleep deprivation had EEG foci, and 17% before and 28% after sleep deprivation had generalized paroxysms. The pathogenesis of epileptic seizures in both groups and the therapeutic consequences are discussed.

The purpose of this study was to find out the value of postoperative EEG controls in the early detection of recurrence of supratentorial gliomas (the majority being astrocytomas, stage II to IV). 29 cases with verified tumour recurrence were examined and in all but one the EEG showed a reactivation of the focus in accordance with the development of the glioma. At least one of the following parameters had to be established: a further spreading of the focal changes, a reduction in frequency, an increase in amplitudes and focal depression of amplitudes. At least 3 postoperative EEG controls were made in each case. The duration of tumour treatment was 3 to 59 months. In 3 cases temporary focus activation was found without evidence of tumour recurrence; in one of these cases the activation was preceded by an epileptic seizure. Epileptic seizures, thus, seem to have a focus activating effect. Focus activation as a result of radiotherapy or cytostatic treatment was not observed. On the basis of our findings it appears that regularly conducted postoperative EEG controls seem to be highly suited as a non-invasive and economical method for the early detection of recurrence of this type of tumour. In the case of malignant types of gliomas involving rapid growth EEG controls should be made monthly.

Both IMP and HMPAO are lipophilic substances with high blood brain barrier permeability and sufficiently long constant retention in the brain parenchyma to enable SPECT to be carried out with a computer controlled Gamma camera. Both tracers are almost completely cleared from the blood during a single passage through the brain. Hence, the regional distribution of activity in the brain is proportional to the regional cerebral blood flow. Computerized acquisition and data processing result in 16 mm thick tomograms at a spatial resolution of 12 mm, which enable clinicians to detect and characterize the pathogenesis and the development of cerebral disorders in terms of altered function. At present, SPECT can be used in daily clinical routine (final SPECT images are available 30 min after the investigation) in cerebrovascular diseases and, because of the coupling of metabolism to cerebral blood flow, in disturbances of cerebral blood flow due to pathological changes of brain metabolism, i.e. in epilepsy and in degenerative disorders. The forthcoming application of physiologically highly specific tracers (e.g. receptor ligands) as a means of studying the distribution of receptors and drugs in the brain will further enlarge the eventual role of SPECT in clinical management.

To assess the value of single photon emission computed tomography (SPECT) in the differential diagnosis of dementia SPECT and conventional computed tomography were performed in 77 patients (50 men, 27 women, mean age 59 [28-90] years) with dementia diagnosed by a battery of psychometric tests. In 13 out of 15 patients with dementia of Alzheimer type SPECT showed a typical Alzheimer pattern (bilateral parietotemporal perfusion defects). Both patients with dementia of Pick type had definite decreases in frontal perfusion. All 21 patients with dementia due to Huntington's chorea showed a typical pattern with absent perfusion of the head of the caudate nucleus, although in three of them conventional computed tomography didn't demonstrate complete atrophy of this structure. Out of 23 patients with multi-infarct dementia there were 17 with focal uptake deficits at various sites, while six displayed an Alzheimer pattern. In Korsakoff's syndrome (n = 11), Down's syndrome (n = 1), Fahr's syndrome (n = 2), senile chorea (n = 1) and HIV encephalopathy (n = 1) no typical distribution patterns were noted. Single photon emission computed tomography can make a contribution to the diagnosis and classification of primary degenerative dementias and can be used to differentiate them from other forms of dementia.

the international classification of epilepsies is presented. This classification is based on pathophysiological, clinical, electroencephalographic, prognostic and therapeutic considerations. The application according to 3 principal types of epilepsies is simple and effective.

Routine determination of the blood serum concentration of most of the usual anticonvulsants is possible by means of an immunoenzymatic method (EMIT). Determination of the total concentration permits conclusions as to the amount of available, unbound and, thus, effective amount of the substance. Regular determination of serum values provides insight into the relevant pharmacokinetics. Metabolism of anticonvulsants differs greatly among individuals and therefore considerable individual variation exists in the relation between the applied dose and the attained serum level. The metabolic rate of the various substances is unequal and, accordingly, the time necessary to reach a steady state and the half life is very variable. Metabolism may be altered by various biological adaptations, diseases or other drugs, causing alterations in the serum level of the anticonvulsant. Results obtained to date indicate a therapeutic threshold concentration range. In a certain percentage of patients seizures are abolished or diminish in frequency only on attaining such a serum level. In more benign cases an adequate therapeutic effect may be obtained with lower ("subtherapeutic") concentrations, while on the other hand, in malignant cases, no efficient control of seizure activity can be attained even at a high serum concentration. The method should be used in all problematic patients. Up to 50% of patients with insufficient control of seizures show improvement or, even, absence of seizures if this method is included in the therapeutic concept.

Fourteen cases of totally or predominantly unilateral ventricular reflux and stasis of intrathecally injected radioisotope or contrast medium were demonstrated by scintigraphy or computed tomographic cisternography. All showed asymmetric enlargement of the lateral ventricles and nine had ipsilateral brain lesions. Four case reports are presented. The pathophysiologic mechanism of communicating hydrocephalus and possible causes of unilateral ventricular reflux are discussed, as well as indications for ventricular shunt installation.

The essentially unspecific EEG-phenomena as expression of the cerebral reaction to extracerebral diseases are described. The most important diseases are dealt with, namely disturbances of the thyroid gland, liver- and kidney disorders, diabetes.

Classification of the hereditary motor and sensory neuropathies is discussed and findings reported in the recent literature are compared to our own findings in a kinship with autosomal dominant CMT. Previous studies in CMT-families with comparable slow nerve conduction velocities had shown positive linkage of this hereditary neuropathy to the Duffy blood group locus; however, blood group typing in the recently studied kinship excluded close linkage, which may indicate the existence of another sub-group in this entity. Testing of visually evoked potentials in this kindred demonstrated significant differences in P 100 latencies of the families of twin brothers. This intrafamilial difference may also be an expression of heterogeneity.

Nosological interpretation and therapy of epileptic psychosis is difficult, since psychotic and epileptic activities are of quite different time relationships. Case reports of two patients suffering from psychosis and showing generalized spike-wave paroxysms, without evidence of clinical seizures, are presented. The problems of diagnosing epileptic psychosis under these circumstances and the therapeutic approach are discussed.

The inability to abstract as an important part of the axial syndrome "Hirnleistungsschwäche" (impairment of intellectual functioning) has been measured by a score system. The score consists of 4 groups of simple questions, the answers of which are given points and added to a total score. A total score of 24.2 +/- 2.4 was obtained constantly in a control group. A preliminary study with patients with cerebro-vascular disease showed a statistically significant reduction in their total score. The clinical usefulness of this score and possible limitations of its use are being discussed.

25 comatose patients suffering from severe cerebral lesions of different etiology were examined during barbiturate-therapy by Glasgow-Pittsburg-Coma-Scoring-System (GPCS), EEG, somatosensory and brainstem acoustic evoked potentials. The findings were correlated in view of prognostic prediction and importance for monitoring. A modified form of the Glasgow-Outcome-Score (GOS; independent-survival, dependent-survival, dead) was used for evaluating the outcome. In case of an initial GPCS less than 10 points none of the patients survived, in case of GPCS greater than 10 points 11 out of 19 patients survived. The latter relation of survival was also found in patients with improving or impairing scores during the observation period. In case of initial burst-suppression pattern in the EEG 7 out of 11 patients survived, in case of diffuse abnormalities with or with-out additional focal signs - 4 out of 10 patients survived, but in the latter there was none with an outcome of independent survival. All patients with an isoelectric EEG died. In case of bilateral recording of scalp- SEP 7 out of 11 patients survived, in case of unilateral loss of scalp-EP 4 out of 8 patients survived, but in the latter cases none with an outcome of independence. All patients with initial bilateral failure of scalp-SSEP or loss during the observation period died. In case of bilateral registrable BAEP (wave I to V) 11 out of 17 patients survived. All patients with initial uni- or bilateral failure of those potentials or loss during the observation period died.(ABSTRACT TRUNCATED AT 250 WORDS)

Extra-intracranial anastomosis are thought to improve the regional cerebral blood flow in patients with a stenosis or occlusion of the carotid system and prevent the later occurrence of ischemic cerebral diseases. Doppler-sonography has been used for a follow up of the effectiveness of the surgical procedure. We believe that minor hemodynamic improvements after surgery cannot be detected by Doppler-sonography. However this method is very useful in demonstrating the patency of the anastomosis.

In 107 patients the EEG after sleep deprivation was performed. The patients have been divided in three groups: 1) with clinically unequivocal, 2) equivocal and 3) no epileptic seizures. All the patients where subdivided in those with and those without anticonvulsive medication. In patients with a previous normal EEG, sleep deprivation had the most activating effect regarding focal or generalized spikes or spike wave complexes in group one. However, patients without medication showed more often activation compared with untreated patients. In the second group the activation was less pronounced, again presenting the same relation between treated and untreated patients. Patients with no seizures as well as a control group of 20 volunteers had no activation at all.

Reflux of 131I-human serum albumin with a dilated ventricle from the contralateral ventricle was observed in a patient with an abnormal cisternogram.

There have been several reports of the isolated occurrence of raised serum gamma GT levels in the course of long-term anticonvulsive treatment. The findings concerning the correlation between this elevation of gamma GT and various dimensions of epilepsy or treatment regimens are equivocal. In a retrospective study of 158 epileptics, the mean values of the serum gamma GT level have been grouped according to anticonvulsive regimen and compared with one another, as well as correlated to the serum concentration of the antiepileptic drug. An elevation of serum gamma GT was found in 103 patients. Among the different subgroups the mean value for serum gamma GT was raised in cases under treatment with PHT, PB or PRM. No such elevation was found in cases under monotherapy with CBZ or VPR. The elevation of serum gamma GT is considered to reflect hepatic enzyme induction rather than hepatic impairment.

The clinical picture of transient global amnesia (TGA) is discussed on the basis of the clinical findings in 19 patients. The central symptom is an acute memory loss, leading to disorientation, helplessness and pseudo-confusion. The symptoms last for several hours and then fade away. Pathogenetically a functional impairment of the limbic system is proposed. Most cases of TGA are due to ischaemic disease; rare causes are epileptic seizures, tumours, encephalitis and toxic or metabolic conditions. In order to clarify the aetiology and initiate appropriate therapy meticulous neurological investigation is necessary. The spontaneous prognosis of ischaemic forms is favourable, whilst in other cases it depends on the primary condition.

A girl with non-contributory family history, at the age of 7 years developed a recurrent ataxic-spastic syndrome followed by disorders of consciousness and seizures. She died in a decerebrate state at the age of 10 9/12 years. Diffuse EEG abnormalities changed in accordance with the clinical course. CSF findings were always negative. Brain biopsy performed at the age of 9 5/12 years was non-diagnostic. No clinical signs of adrenal insufficiency were present. Neuropathological examination disclosed severe demyelination of the cerebral white matter with formation of large periventricular cavities, relative sparing of the subcortical arcuate fibers, and peripheral myelin breakdown of the orthochromatic (neutral fat) type. There was complete absence of inflammatory lesions, comparative preservation of axons and oligodendroglia with moderate astroglial reaction. The optic system and cerebellum were not involved. Additional postanoxic changes were seen in the thalamus and hippocampus. The sporadic case is suggested to represent a cavitating form of neutral fat (simple orthochromatic) leukodystrophy which is to be separated from Schilder's diffuse sclerosis and adrenoleukodystrophy. The etiology of the disorder is unknown.

21 comatose patients were examined by somatosensory evoked potentials (SSEP). The findings were correlated with the stage of brainstem herniation, the EEG and the outcome. We evaluated the early components of the SSEP (N10, N13, N14, P15, N20) in view of presence, latency and interpeak-latency of the potentials. In most cases the percentage of abnormal SSEP increased from caudal to rostral registration sites, but the potential P15 and N20 were equally abnormal. The progression of herniation correlated with increasing abnormality of the potentials. SSEP over the scalp (P15, N20) could not be registered in patients without any EEG-activity (isoelectric). Mean values of latencies and the interpeak-latencies were significantly prolonged in all cases with fatal outcome. Our findings suggest SSEP as a useful tool in the evaluation of brain-dysfunction in comatose patients.